The ability of chlorinated hydrocarbons to induce uterine ornithine decarboxylase (ODC) in the rat as a measure of estrogenicity of these compounds, was further explored. Utilizing ovariectomized rats instead of intact rats it was shown that the sensitivity of the assay was markedly increased and that a single dose as low as 2 mg/kg B.W. demonstrated estrogenic activity. Compounds, such as p,p'DDD and p,p'DDE, which were inactive in various estrogenic assays, were active (low activity) in the ODC induction assay. Tamoxifen, a typical antiestrogen, given to rats inhibited the induction of ODC by o,p'DDT, demonstrating the estrogenic nature of this chlorinated hydrocarbon. An attempt to determine whether o,p'DDT was active per se or through a metabolite, has yielded hitherto only equivocal results. It was shown that o,p'DDT interference with the binding of estradiol to uterine estrogen receptor was due to competition for the binding sites and not due to destruction of the receptor. Furthermore, we found that the administration of o,p'DDT to rats elevates the estrogen binding sites in the nucleus; this finding further demonstrates that o,p'DDT is acting as a typical estrogen. BIBLIOGRAPHIC REFERENCES: D. Kupfer and W.H. Bulger, Inhibition by CC14 of the o,p'DDT and Estradiol (E2)-Mediated Induction of Rat Uterus Ornithine Decarboxylase (ODC), Abstract submitted to 1976 FASEB. D. Kupfer, Effects of Pesticides and related compounds on steroid metabolism and function, CRC Critical reviews in Toxicol. 4, (#1). 83 (1975).